GP Flashcards
(184 cards)
1
Q
What are the two main categories of pruritus (itch)?
A
Dermatological and systemic causes.
2
Q
What are common dermatological causes of itch?
A
Eczema, psoriasis, urticaria, scabies, contact dermatitis, lichen planus.
Fungal stuff
asteatotic eczema in older people, due to moisture loss of the skin
3
Q
What are common systemic causes of itch?
A
Liver disease (cholestasis), renal disease, haematological disorders, endocrine disorders, neuropathic causes, psychogenic causes.
4
Q
Which systemic conditions can cause generalised itch?
A
Liver disease, chronic kidney disease, lymphoma, iron deficiency, thyroid dysfunction, diabetes, neurological disorders.
5
Q
Which haematological conditions can cause pruritus?
A
Polycythaemia vera, Hodgkin’s lymphoma, iron deficiency anaemia.
Low iron levels can lead to dry skin and increased sensitivity of nerve endings, resulting in generalized itching.
Hematologic Disorders (e.g., Polycythemia Vera) – Excess red blood cell production can increase blood viscosity, leading to histamine release and itching, especially after hot showers.
Malignancies (e.g., Lymphoma, Leukemia) – Cancers like Hodgkin’s lymphoma can cause severe pruritus due to immune system activation and release of inflammatory mediators.
6
Q
What are red flag symptoms associated with itch?
A
Weight loss, night sweats, fever, lymphadenopathy, jaundice, dark urine, pale stools.
7
Q
Which liver conditions commonly cause pruritus?
A
Primary biliary cholangitis, cholestasis of pregnancy, obstructive jaundice.
Conditions like cirrhosis and bile duct obstruction lead to bile salt accumulation, which irritates nerve endings and causes severe itching, often worse at night.
8
Q
Which renal condition is a major cause of pruritus?
A
Chronic kidney disease (uremic pruritus).
Impaired kidney function leads to the buildup of toxins in the blood, which can cause persistent itching, especially on the back and limbs.
9
Q
What are common medications that can cause pruritus?
A
Opioids, ACE inhibitors, NSAIDs, statins, chloroquine, hydroxychloroquine.
10
Q
waht are some obs causes of itch
A
Intrahepatic cholsetatsis of pregnacy
HELP syndrome
Polymorphic erruption of pregnacy
11
Q
What is the characteristic feature of scabies-related itch?
A
Worse at night, often involves finger webs, wrists, and genitals, presence of burrows.
small red burrows
12
Q
What skin condition presents with itchy, silvery plaques on extensor surfaces?
A
Psoriasis.
13
Q
What are typical features of atopic eczema?
A
Dry, itchy, inflamed skin, often in flexural areas (elbows, knees, neck).
14
Q
What is the first-line treatment for pruritus due to eczema?
A
Emollients:
- E45 (thinner)
- Aveeno (oatmill oil, not petrollerum jelly)
- Diprobase (thinner)
Oilatum (thicker)
Topical steroids
Steroids
- Dermovate (most potent, palms and soles only)
- Eumovate
- Elocon
- Betnovate
- Hydrocortisone (weakest)
Higher potency for shorter, is better for skin
15
Q
What is the first-line treatment for urticaria?
A
Oral antihistamines
Antihistamines
- Chlorphenamine /Piriton (sedative)
- Fexofenadine / Telfast (non sedating)
- Loratadine - (non sedating) - Cetirizine - (non sedating) .
16
Q
How is scabies treated in primary care?
A
Permethrin 5% cream applied to the whole body, repeated after 7 days.
17
Q
What investigations would you request for persistent generalised itch?
A
FBC, LFTs, U&Es, TFTs, iron studies, CRP/ESR. Ferritin
18
Q
What additional tests might be needed if pruritus is unexplained?
A
HIV test, hepatitis panel, ANA (autoimmune diseases), skin biopsy (if dermatological cause suspected).
19
Q
How does cholestatic pruritus typically present?
A
Generalised itch, worse on palms and soles, associated with jaundice, pale stools, and dark urine.
20
Q
How is pruritus in chronic kidney disease managed?
A
Emollients, antihistamines, gabapentin, optimising dialysis.
21
Q
What are some key non-dermatological causes of nocturnal pruritus?
A
Scabies, liver disease, iron deficiency, psychogenic pruritus.
22
Q
What is a common psychological cause of pruritus?
A
Stress-related pruritus or delusional parasitosis.
23
Q
Why is a thorough medication review important in a patient with generalised itch?
A
Certain drugs (opioids, NSAIDs, ACE inhibitors) can trigger pruritus.
24
Q
What is the role of antihistamines in the management of itch?
A
Effective for histamine-mediated conditions (urticaria, allergic reactions) but less effective for systemic pruritus.
25
What topical treatments are commonly used for pruritus?
Emollients, menthol creams, topical steroids (if inflammation present).
26
How does pruritus due to Hodgkin’s lymphoma typically present?
Generalised itch with B symptoms (fever, weight loss, night sweats).
27
Which condition is associated with aquagenic pruritus?
Itching in contact with water
Polycythaemia vera.
28
What is the Fitzpatrick skin type system, and why is it important in dermatology?
It classifies skin types based on their response to sun exposure; helps recognise skin conditions in different skin tones.
29
Name some causes of cauda equina syndrome
Herniation of lumbar disc – most commonly at L4/L5 and L5/S1
Spondylolisthesis – most commonly anterolisthesis (vertebra moves forward)
Trauma – car crash, gun shot, bleeding via haematomas
Tumours
Infection
Post-op haematoma
30
Causes of cauda equina syndrome - what is spondylolisthesis? What pathophysiological effects will be seen as a result of spondylolisthesis?
Spondylolisthesis is where one of the bones in your spine, called a vertebra, slips forward
most commonly anterolisthesis (vertebra moves forward)
Slippage of one vertebra over the one below
Nerve root comes out ABOVE the disc therefore root affected will be the one BELOW the disc herniation
E.g. L4/L5 herniation 🡪 L5 nerve root compression
31
What are some symptoms/signs of cauda equina syndrome
***Saddle anaesthesia***
Less bladder and bowel control – increased tone of anal sphincter and muscle wall of bladder
Erectile dysfunction (or other sexual dysfunction)
Lumbosacral pain
Leg weakness – flaccid and areflexic
Paraplegia
Bilateral symptoms
feeling like you need the toilet, and urethral sensation (feels like you are passing urine) - **precursor to incontintence, is a red flag**
Signs
Areflexia
Fasciculations
Loss of bowel/bladder control
Urinary retention
**WILL SEE LOWER MOTOR NEURON SIGNS ONLY***
32
What are some investigations for cauda equina syndrome?
MRI spinal cord (diagnostic)
PR exam - feel for any abnormalities, and check anal tone
Testing nerve roots/reflexes
Knee flexion – test L5-S1
Ankle plantar flexion – test S1-S2
Straight leg raising – L5, S1
Femoral stretch test – L4
33
What is the management for cauda equina syndrome?
Management
Refer to neurosurgeon ASAP to relive pressure
Surgical decompression
High dose dexamethasone
Corticosteroids
34
what is the management of sciatica?
. Conservative Management (First-Line)
Pain Relief: NSAIDs (e.g., ibuprofen) or paracetamol; consider neuropathic agents (e.g., **amitriptyline,** gabapentin) if needed.
Physical Therapy: Stretching, strengthening, and core exercises.
Activity Modification: Avoid prolonged sitting, maintain gentle movement.
Heat/Ice Therapy: May help alleviate symptoms.
35
Prescribing - What do you need to give w NSAIDs in over 50s?
What do you not give to ashmatic
PPI as well
dont give naproxen to asthmatics
36
what are the Causes of Sciatica
Sciatica occurs when the sciatic nerve (which runs from the lower back down to the legs) is compressed or irritated. Common causes include:
Herniated Disc – A slipped/prolapsed disc in the lumbar spine pressing on the nerve.
Spinal Stenosis – Narrowing of the spinal canal, often due to aging.
Piriformis Syndrome – Tightness or spasm of the piriformis muscle compressing the sciatic nerve.
Spondylolisthesis – A vertebra slips out of place, compressing the nerve.
Trauma/Injury – Direct damage to the lower back or sciatic nerve.
Tumors or Infections – Rare, but can put pressure on the nerve.
37
What is a SR 1 form
SR1 - maximum levels of benefit - no questions asked, usually have around 6 months to live
38
outline pain prescribing ladder
Simple analgesics - NSAIDS, Paracetamol
Step 3: Add codeine/co-codamol (weak opioids) 30-60mg every 4 hours
Step 4: Stop codeine/co-codamol & trial tramadol (weak opioid) initially 100mg, then 50-100mg every 4-6 hours, cam
Step 6: Stop tramadol & start morphine
Typical drug dosing for (oral) morphine:
Acute pain: initially 10mg every 4 hours; use a lower initial dose in the elderly (5mg every 4 hours)
Chronic pain: 5-10mg every 4 hours
Step 7: Refer to pain management specialists
39
What kind of laxatives would you use?
Osmotics/softeners
laxido/movicol, one sachet BD - really foul, neck
Lactulose (syrup)
Stimulant
Senna (tablets)
Usually avoid bulking laxatives (fybogel/isapghula husk)
40
What are some specific considerations for codeine, tramadol/morphine
Codeine - very good at casuing constipation
Tramadol - can cause vivd dreams, weird psychiatric issues, especially in the eldery
41
What are the types of morphine medications
1. Immediate-Release (IR) Morphine
For acute pain relief
Examples: Oramorph, Sevredol
2. Extended-Release (ER) / Controlled-Release (CR) Morphine
For chronic pain management
Examples: MST Continus, Kadian, MS Contin
3. Injectable Morphine
For severe pain, often used in hospitals
4. Epidural & Intrathecal Morphine
For spinal pain relief, used in surgery or cancer pain
Example: Preservative-free morphine
42
Outline the dispensing of neuropathic pain
Amitriptyline
Gabapentin
Pregabalin
Duloxetine - often used for diabetic neuropathy
43
What is the inital dosing and side effects of pregaalin and gabapentin
Typical drug dosing (oral) pregabalin:
Peripheral and central neuropathic pain: initially 150mg daily in 2-3 divided doses; then titrated up according to the BNF
Typical drug dosing (oral) gabapentin:
Peripheral neuropathic pain: initially 300mg once daily; then titrate up according to the BNF
Doses should be reduced in patients with renal impairment.
Use Gabapentin before pregabulin
Drowsiness
Dizziness
Ataxia
These usually improve in the first few weeks of treatment.
44
What is an advanced decision?
What is an advanced statement?
When are advanced statements particulary relevant?
An Advanced Decision, short for Advanced Decision to Refuse Treatment, is a legally binding document. Its purpose is to ensure that an individual can refuse a specific treatment(s) that they do not want to have in the future.
An Advance Statement is sometimes called a "Statement of Wishes and Care Preferences". It allows an individual to make general statements about their wishes, beliefs, feelings and values and how these influence their preferences for their future care and treatment.
An Advance Statement is not by itself legally binding, but legally must be taken into consideration when making a "best interests" decision on someone's behalf under the Mental Capacity Act (MCA), 2005. This is because one of the criteria of the MCA is that a patient's "wishes, feelings, beliefs and values" must be taken into consideration; an Advanced Statement provides evidence of this.
45
What is a Lasting power of attorney??
“A document which a person can nominate someone else to make certain decision on their behalf (for example on finances, health and personal welfare) when they are unable to do so themselves”.
To be valid, it needs to be registered with the Office of the Public Guardian
46
What is an Independent mental capacity advocate (IMCA) ?
Commissioned from independent organisations by the NHS and local authorities to ensure that MCA is being followed
Role of IMCA: support and represent people who lack capacity and they do not have anyone else to represent them in decisions about changes in long-term accommodation or serious medical treatment. They can also be present for decisions regarding care reviews or adult protection.
47
Oultine what an advanced decsions to refuse treatment is
An Advance Decision to Refuse Treatment (ADRT) is a legally binding statement where a person (with capacity) refuses specific medical treatments in advance, in case they lose capacity in the future.
Key Components of an ADRT:
Specific Treatments Refused – Must clearly state which treatments are declined (e.g., CPR, ventilation).
Applicable Situations – Defines when the refusal applies (e.g., terminal illness, coma).
Capacity & Voluntariness – Must be made when the person has mental capacity.
Life-Sustaining Treatment Refusal – Must be in writing, signed, and witnessed.
Review & Updates – Should be reviewed regularly to ensure relevance.
ADRTs must be followed unless there is doubt about validity or applicability.
48
Outline what a respect form is
ReSPECT Form (Recommended Summary Plan for Emergency Care and Treatment)
A ReSPECT form records a person’s preferences and clinical recommendations for emergency treatment if they lose capacity. It helps guide healthcare decisions, including CPR.
Key Features:
Personalized emergency care plan based on patient wishes & clinical judgment.
Includes CPR decisions but is broader than a DNACPR.
Shared decision-making between patient and healthcare professionals.
Non-legally binding but should be respected by clinicians.
Portable document used across different care settings.
49
Explain the use of and the differences between an ‘advance statement’, ‘Lasting
power of attorney’ and an ‘advanced decision to refuse treatment’
Advance Statement:
Records general preferences for care (e.g., diet, religious beliefs).
Not legally binding, but should be considered by clinicians.
Advance Decision to Refuse Treatment (ADRT):
Legally binding refusal of specific medical treatments.
Must be specific, valid, and applicable (life-sustaining refusals need a signature & witness).
Lasting Power of Attorney (LPA) for Health & Welfare:
Appoints a trusted person to make healthcare decisions if capacity is lost.
Legally binding once registered, can include life-sustaining treatment decisions.
50
What are some preemptive prescribing options for pain - give doses
Pre-emptive Prescribing with Basic Dosages
1. Pain (e.g., Morphine)
○ Morphine 10mg oral every 4 hours as needed
○ Morphine 2.5-5mg subcutaneous every 4 hours as needed
Give Oxycodone if eGFR is <30
51
What are some preemptive prescribing options for breathlessness - give doses
Breathlessness (e.g., Morphine or Midazolam)
○ Morphine 2.5-5mg subcutaneous every 4 hours as needed
52
What are some preemptive prescribing options for agitation - give doses
3. Agitation (e.g., Midazolam or Levomepromazine)
○ Midazolam 2.5-5mg subcutaneous every 4 hours as needed
○ Levomepromazine 6.25-12.5mg oral or subcutaneous every 8 hours as needed (use in a driver, very sedating)
53
What are some preemptive prescribing options for nausea - give doses
4. Nausea/Vomiting (e.g., Levomepromazine or Haloperidol)
○ Levomepromazine 6.25-12.5mg oral or subcutaneous every 8 hours as needed (use in a driver, very sedating)
○ Haloperidol 1-2mg oral or subcutaneous every 8 hours as needed
Dompiridone - anti sickness used in parkinosns as it doesn't cross the BBB
54
What are some preemptive prescribing options for secretions - give doses
5. Respiratory Secretions (e.g., Glycopyrronium or Hyoscine Butylbromide)
○ Hyoscine Butylbromide 20mg subcutaneous every 4 hours as needed - dries up secretions, do mouthcare!
55
What is the management for a TIA?
Immediate management
Immediate loading dose: Aspirin 300mg
Refer to specialist – to be seen within 24h of symptom onset
Dual Antiplatelet therapy
Standard treatment is Aspirin 75mg daily
With modified-release Dipyridamole
OR Clopidogrel daily
Dont give aspirin if history of GI issues for risk of bleeding, NICE advises just clopipedergrel
56
What is the acute management for a TIA?
What procedure is done?
- **Antiplatelet:** initially aspirin 300mg - the first-line, immediate management, if aspirin not appropriate, give an Clopidergol
(give PPI as well w aspirin)
**REFER TO STROKE SPECIALIST***
**Carotid endarterectomy:** surgical procedure to remove the blockage, Done within 2 weeks stenosis of > 70% on Doppler is an indication for urgent endarterectomy
57
What further management can you provide for a TIA after the acute antiplatelets?
What are the driving rules
A High-intensity Statin - atorvastatin : 20-80 mg orally once daily
An anticoauglant for AF - eg A low molecular weight heparin eg dalteparin, or
A direct thrombin inhibitor or factor Xa inhibitor - rivaroxaban
Give aspirin 300mg OD for 2wks, then switch to clopidogrel 75mg OD.
Driving Rules After a TIA (UK DVLA Guidelines)
Group 1 (Car/Motorcycle): Must stop driving for at least 1 month. Can resume if fully recovered and no further TIAs. No need to inform DVLA unless there are recurrent events.
Group 2 (Lorry/Bus): Must stop driving for at least 1 year. Must inform DVLA and can only resume if medically assessed as fit.
58
What are the common causes of salivary gland stones?
Salivary stasis, high calcium/phosphate, mucous plugs, chronic inflammation, medications (anticholinergics, diuretics), metabolic disorders (gout, hypercalcaemia).
59
What are the key signs and symptoms of sialolithiasis?
Pain and swelling in the affected gland, worse with eating, tenderness, palpable stone (if near duct), dry mouth, possible secondary infection (redness, pus).
60
What investigations help diagnose salivary gland stones?
Clinical exam (bimanual palpation), X-ray (radio-opaque stones), ultrasound (detects non-radiopaque stones), sialography (recurrent cases), CT (if deep/multiple stones).
61
How is sialolithiasis managed in general practice?
Conservative: Hydration, sialogogues (citrus/gum), gland massage, pain relief. If infected: Antibiotics (flucloxacillin ± metronidazole), warm compresses.
62
When should a patient with salivary gland stones be referred to ENT?
Large/deep/recurrent stones, persistent obstruction & pain, recurrent sialadenitis or abscess, failed conservative treatment.
63
Blood in Atypical pneumonia
Low Sodium, and Deranged intrahepatic LFTs
64
Causes of Derranged LFTS
Hepatocellular Injury (↑ALT/AST > ALP):
Viral hepatitis (A, B, C, etc.)
Alcoholic hepatitis
Non-alcoholic fatty liver disease (NAFLD/NASH)
Drug-induced liver injury (e.g., paracetamol, statins)
Autoimmune hepatitis
Ischemic hepatitis (shock liver)
Wilson’s disease, hemochromatosis, alpha-1 antitrypsin deficiency
Cholestatic Pattern (↑ALP/GGT > ALT/AST):
Biliary obstruction (stones, stricture, tumour)
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Drug-induced cholestasis
Infiltrative diseases (e.g., sarcoidosis, lymphoma)
Mixed Pattern:
Drug-induced
Alcoholic hepatitis
Sepsis-related cholestasis
65
Typical bloods in an alcoholic
Typical Blood Results in Chronic Alcohol Use:
Liver Function Tests (LFTs):
↑ AST > ALT (usually AST:ALT ratio > 2:1; due to mitochondrial damage and B6 deficiency)
↑ GGT (highly sensitive to alcohol use)
↑ ALP (mildly elevated if cholestasis present)
↑ Bilirubin (in advanced liver disease)
Full Blood Count (FBC):
Macrocytic anemia (↑ MCV) — due to folate/B12 deficiency or direct alcohol toxicity
Thrombocytopenia — due to hypersplenism or bone marrow suppression
Leukopenia — in severe liver disease or bone marrow suppression
Coagulation Profile:
↑ INR/PT — impaired hepatic synthesis of clotting factors
Others:
↓ Albumin — reduced hepatic synthetic function
↑ Ammonia (in hepatic encephalopathy)
↑ Ferritin — acute phase reactant and liver injury
↓ Glucose — in advanced liver disease or alcoholic hypoglycemia
66
What is the key pathological difference between bronchiectasis and COPD?
Bronchiectasis involves permanent dilation of bronchi due to chronic infection and inflammation, while COPD is characterized by airflow obstruction due to emphysema and chronic bronchitis.
67
What are the main causes of bronchiectasis and COPD?
Bronchiectasis is often caused by recurrent infections, cystic fibrosis, or immune deficiencies. COPD is mainly caused by smoking, air pollution, and chronic exposure to irritants.
68
How does sputum production differ in bronchiectasis vs COPD?
Bronchiectasis typically produces large volumes of thick, purulent sputum, whereas COPD sputum is usually mucoid and varies in quantity.
69
What are the characteristic symptoms of bronchiectasis compared to COPD?
Bronchiectasis presents with chronic productive cough, frequent infections, and hemoptysis, while COPD presents with chronic cough, progressive dyspnea, and wheezing.
70
What auscultation findings help differentiate bronchiectasis from COPD?
Bronchiectasis may have coarse crackles and wheezing, while COPD is characterized by wheezing, prolonged expiratory phase, and reduced breath sounds in advanced stages.
71
What imaging modality is best for diagnosing bronchiectasis and what would it show?
High-resolution CT (HRCT) is the gold standard for bronchiectasis, showing dilated bronchi with a 'tram-track' or 'signet-ring' appearance.
72
How is COPD typically diagnosed?
COPD is diagnosed using spirometry, showing an FEV1/FVC ratio < 0.7, indicating irreversible airflow obstruction. FEV1/FVC ratio normal in COPD
73
What are the main treatment differences between bronchiectasis and COPD?
Bronchiectasis treatment focuses on airway clearance (physiotherapy, postural drainage), antibiotics for infections, and mucolytics, whereas COPD is managed with bronchodilators, corticosteroids, smoking cessation, and oxygen therapy in severe cases.
74
What role do infections play in exacerbations of bronchiectasis and COPD?
Infections are a major cause of exacerbations in both, but bronchiectasis patients often have chronic colonization (e.g., Pseudomonas), whereas COPD exacerbations are commonly caused by bacterial or viral infections.
75
How does the response to bronchodilators differ in bronchiectasis vs COPD?
COPD typically responds to bronchodilators, while bronchiectasis has limited bronchodilator response and is more reliant on airway clearance techniques.
76
What is the key pathological difference between frozen shoulder and shoulder tendonitis?
Frozen shoulder (adhesive capsulitis) involves thickening and contraction of the shoulder capsule, leading to stiffness. Tendonitis is inflammation of the tendons, often due to overuse or impingement.
77
What are the common causes of frozen shoulder and tendonitis?
Frozen shoulder is often idiopathic but associated with diabetes and prolonged immobilization. Tendonitis is usually caused by repetitive overhead activity, trauma, or degenerative changes.
78
Why can calcifications develop in shoulder tendons?
Calcium deposits form due to chronic tendon irritation, hypoxia, or degeneration, most commonly in calcific tendinitis of the rotator cuff (especially the supraspinatus tendon).
79
What specific examination findings are seen in frozen shoulder?
Global restriction of both active and passive shoulder movement, especially external rotation, with pain at end range.
80
What specific examination findings suggest tendonitis?
Pain with resisted movements, such as painful arc (60–120° abduction), tenderness over the affected tendon.
81
How does pain presentation differ in frozen shoulder vs tendonitis?
Frozen shoulder has a progressive, diffuse pain pattern with increasing stiffness, whereas tendonitis presents with localized pain, especially with overhead activity.
82
What is the treatment for frozen shoulder
NSAIDs, paracetamol, or oral steroids for pain; intra-articular steroid injection for relief; physiotherapy with gentle ROM exercises; hydrodilatation if severe; MUA or arthroscopic release for refractory cases.
83
Which patients are most at risk of developing frozen shoulder?
Diabetics, patients with thyroid disorders, or those with prolonged shoulder immobilization (e.g., post-surgery or fracture).
84
How can bronchiectasis lead to heart failure
Airways that are full of mucous become hypoxic.
Widespread hypoxia leads to widespread vasoconstriction of the pulmonary blood vessels - leading to pulmonary hypertension
Pulmonary hypertension means that the right side of the heart will have to beat harder to get blood around pulmonary circulation - RV hypertrophy
Known as Cor pulmonale
85
Define lymphoma - what does it lead to?
Malignant proliferation of lymphocytes which accumulate in lymph nodes 🡪 lymphadenopathy
86
What are the risk factors of Hodgkin's Lymphoma?
- **Bimodal age distribution**: 15-35 years and > 60 years
- **Epstein Barr Virus**: mixed cellularity subtype
- **HIV infection:** lymphocyte-deplete subtype
- **Autoimmune conditions** such as rheumatoid arthritis and sarcoidosis
- **Family history**
87
What are some signs and symptoms of Hodgkinsons lymphoma?
- **Lymphadenopathy** (may be cervical, axillary, or inguinal)
- **Painless**
- Hard
- Rubbery
- Fixed
- Contiguous spread (to nearby nodes) unlike in NHL
- **Splenomegaly**: rarer compared to NHL
- **B symptoms**: occur in around 30% of cases
- **Fever**
- **Weight loss**
- **Night sweats**
- **Pel-Ebstein fever:** an intermittent fever every few weeks
- **Alcohol-induced lymph node pain**
- **Pruritus**
- **Dyspnoea:** due to mediastinal lymphadenopathy
88
What is the Hallmark cell to diagnose Hodgkin's lymphoma?
What antigens are almost always expressed on these cells?
Reed-Sternberg cell (aka lacunar histiocytes). These are giant malignant cells seen on light microscope
CD15 and CD30 antigens are almost always expressed on these cells in HL.
**USED TO DISTINGUISH BETWEEN HODGKIN AND NON HODGKIN LYMPHOMA**
*Picture credit unknown*
89
What investigations would you do for Hodgkin's Lymphoma?
CT/MRI of chest, abdomen and pelvis – show staging (Ann Arbor)
**Lymph node biopsy** and histological examination - shows Reed-Sternberg cells
FBC – may be normal of show normochromic, normocytic anaemia
CXR
WCC is often not raised in HL!!
90
Investigating Lymphoma - What is the Ann Arbour Staging? What does it focus on? How many stages are there
**Used in Both Hodgkin's and Non - Hodgkin's Lymphoma**
Its a system that looks at whether affected nodes are above or below diaphragm. Done on **CT/MRI**
There are 4 stages - **USED TO GUIDE TREATMENT**
91
What are the main differences between Hodgkin and non Hodgkin lymphoma?
Hodgkin’s -
- **Contiguous** *(only spreads to adjacent nodes/structures, due to flow of Lymph)* - ***rarely extra nodal***
-Affects a particular type of B-cell: **Reed-Sternberg Cells**
-**Younger age of onset**
- **Painful nodes on drinking alcohol**
-**Better Prognosis than Non - Hodgkin Lymphoma**
Non-Hodgkin’s -
**Non-contiguous** *(multi-centric - can arise in several unlinked structures,)* - ***extra nodal***
**No RS cells**
Older age of onset (7th decade)
-**Worse Prognosis than Hodgkin Lymphoma**
92
What is the management of later stage Hodgkinson Lymphoma?
What does relapse respond well to?
A **Longer course of Chemo** ,
And radiotherapy
Relapse responds well to autologous bone marrow transplantation
93
What is Non Hodgkin's lymphoma?
What cells do the tumours originate from
These are malignant tumours of lymphoid tissue, that do not contain Reed-Sternberg cells
70% are B cell in origin
30% are T cell in origin
*"This includes all lymphomas without Reed–Sternberg cells —a diverse group"*
94
What is more common and HL or NHL and what is the most common type of lymphoma overall?
NHL is far more common
B-cell lymphoma are more common that T-cell lymphomas
95
What are some signs of Non hodgkin lymphoma?
- **Lymphadenopathy**
- **Painless**
- Hard
- Rubbery
- Fixed
- Non-contiguous spread unlike in HL
- **Splenomegaly:** more common in NHL compared to HL
- **Extranodal disease:** bone marrow, thyroid, salivary gland, GI tract, CNS
*B symptoms**:
- Fever
- Weight loss
- Night sweats
- Related to extranodal involvement:
- GI tract: **bowel obstruction**
- Bone marrow: **fatigue, easy bruising, or recurrent infections**
- Spinal cord: **weakness and a loss of sensation - usually in the legs**
96
What investigations would you do in suspected non Hodgkin lymphoma
CT – for staging
Lymph node biopsy - **no Reed-Sternberg Cells**
FBC - *could show Anaemia, Elevated WBC or thrombocytopenia, Raised ESR -(Erythrocyte sedimentation rate)
CXR
PET scan
BM aspirate and trephine biopsy to confirm marrow involvement
97
What is the management for Non - Hodgkin Lymphoma?
Steroids
**Rituximab** - *targets CD20 on B cells*
CHOP regimen: (A Chemotherapy regimen)
Cyclophosphamide
Hydroxy-daunorubicin
Vincristine
Prednisolone
98
Treatment for Non - Hodgkin lymphoma - what is Rituximab, and what does it do?
Rituximab: monoclonal antibody targets CD20 on lymphocytes and is used in CD20+ lymphoma
99
What are the most common antibodies that there ends up being large amounts of in the blood in myeloma?
IgG (2/3) and IgA (1/3)
100
Outline the pathophysiology of a myeloma
There is clonal proliferation of the plasma cells
Normally plasma cells produce a wide range of immunoglobulins (antibodies) such as IgG, IgA, IgM and IgD
In myeloma, malignant plasma cells produce an **excess of one type of immunoglobulin**usually IgG and IgA.
Bence Jones protein deposition in urine
101
Pathophysiology of myeloma - what is the name given to the specific type of antibody that is specifically produced by the malignant plasma cell?
what do these neoplastic plamsa cells do that can lead to symptoms?
***monoclonal paraprotein***
(only consisting of light chains rather than a light and heavy chain)
Neoplastic cells release Cytokines, that lead to **activating of osetoclasts via RANKL**
Light chains from the pathological antibodies **Known as Bence Jones proteins** can interrupt/impair renal function
Bone marrow can get infiltrated by plasma cells - reduced haematopoesis, leading to **anaemia**
102
What are the symptoms of Myelomas?
***CRAB***
Calcium raised (Hypercalcaemia) cancer symptoms, Confusion (hyperviscosity, hypercalcaemia), repeat infections, pathological fractures
Renal failure – nephrotic syndrome
*Immunoglobulin light chains deposit in organs especially kidneys*
**Anaemia, infections and bleeding** due to BM infiltration (anaemia, thrombocytopenia, leukopenia)
Bone pain – increased osteoclastic activity cause bone destruction (backache most common symptom)
Osteolytic lesions, easy fractures, Spinal cord compression
***CRAB***
***NICE suggest considering myeloma in anyone over 60 with persistent bone pain, particularly back pain, or an unexplained fractures!!!!!***
103
What are the investigations for suspected myeloma?
**FBC** (low white blood cell count in myeloma)
**Calcium** (raised in myeloma)
**Erythrocyte sedimentation rate** (raised in myeloma)
Plasma viscosity (raised in myeloma)
**B – Bence–Jones protein (request urine electrophoresis)**
L – Serum‑free Light‑chain assay
I – Serum Immunoglobulins
P – Serum Protein electrophoresis
**Raindrop skull on xray** - random patterns of dark spots on skull
***Rouleax formation*** - the stacking of RBC on blood film
Electrophoresis = separating molecules based on charge
**Bone marrow biopsy** is necessary to confirm the diagnosis of myeloma
104
What are some common causes of atrial fibrillation?
PE/COPD
IHD, Heart failure
Rheumatic heart disease, Valve abnormalities
Alcohol intake
**Thyroid issues - Hyperthyroidism**
Sleep Apnoea
Electrolyte disturbances - Hyper/Hypo Kalaemia, Hypo magnesia
PIRATE
105
What are some signs and symptoms of AF?
- **Irregular irregular pulse**
- **Hypotension:** red flag; suggest haemodynamic instability
- **Evidence of heart failure:** red flag; such as pulmonary oedema
- **Palpitations**
- **Dyspnoea**
- **Chest pain:** red flag
- **Syncope:** red flag
Can also be asymptomatic!
106
What is the first line management for someone who is haemodynamically stable with AF? What signs could indicate that this is the case? What Rate control would you do?
Start by controlling either **rate of rhythm**
Rate control:
- **First line: beta-blocker** (e.g. bisoprolol) or a **rate-limiting calcium-channel blocker** (e.g. verapamil)
- **Digoxin**: may be considered first-line in patients with AF and heart failure
**In AF, aim to keep HR under 100**
***IF HAEMODYNAICALLY STABLE, DO RATE CONTROL BEFORE RHYTHM CONTROL***
Start very low w BB
107
Anticoagulants are often given to patient with AF to reduced their likelihood of developing clots that can cause strokes.
What scoring system is used to calculate stroke risk in AF? What types of factors are included on it?
**CHADS2VASc** score used to calculate stroke risk in AF
0 = no anticoagulation
1 = consider oral anticoagulation or aspirin
2 = Anticoagulants - **DOACS** - Apixaban to reduce risk of strokes
Congestive Heart failure = 1
Hypertension = 1
Age > 75 = 2
Age 65-74 = 1
Diabetes Mellitus = 1
Stroke or TIA = 2
Vascular disease = 1
Female sex = 1
108
What would you see on an ECG for someone in AF?
Irregularly irregular
F (Fibrillatory) waves
No clear P waves
Rapid QRS complex
absence of [isoelectric]
baseline
variable ventricular rate
109
What Rhythm control would you do in AF?
When would you do rhythm control first?
Rhythm control: - *either pharmacological or electrical cardioversion*
- **Pharmacological: - anti-arrhythmics**
- **Flecainide or amiodarone**: if no evidence of structural/ischaemic heart disease
- **Amiodarone**: if structural/ischaemic heart disease is present
- **Electrical cardioversion:** rapidly shock the heart back into sinus rhythm
***IF HAEMODYNAICALLY UNSTABLE, DO RHYTHM CONTROL BEFORE RATE CONTROL (aka Cardioveresion)***
Do rhythm control first if an acute episode (presents in 48 hours)
if the AF is causing heart failure
In younger patients
110
Give some differentials for causes of a fall
Syncope
Trip
vision
rhythm
TIA/CVA
MSK
Parkinsons/Alzheimers
Mets from Ca
Infection in someone whose frail
Epilepsy
meds
111
Some management of a fall as F1 at 3am
look at notes - PMH, medications, baseline cognition
ICE - recent blood tests
Speak to them, history.
Neuro assessment/exam needs to rule out TIA
BM?
ECG for weird heart issues
News2 - Sepsis protocol
Think about t
Seizures, TIA
112
explain differences between chadvas and orbit scores
Summary
CHA₂DS₂-VASc → Decides if a patient needs anticoagulation.
ORBIT → Assesses how risky anticoagulation is.
Both scores should be used together to balance stroke prevention vs. bleeding risk in AF management.
Would you like a clinical example of how to apply both scores in decision-making?
113
what are the criteria of orbit scoring
Age >75 - point
reduced haemoglobin (<13 mg/dL in men and <12 mg/dL in women), haematocrit (<40% in men and <36% in women) or history of anaemia - 2 point
Bleeding history - 2 point
insufficient kidney function (eGFR < 60 mg/dL/1.73 m2) - 1 point
treatment with an antiplatelet agent - 1 point
0-2 = 2.4%
3 = 4.7%
4-7 = 8.1%
114
What is DOLS?
Deprivation of Liberty Safeguards.
DOLS are part of the MCA, the safeguards aim to ensure that people in care homes or hospitals who lack capacity are looked after in a way that has their best interests at heart.
115
What questions should be asked when determining whether something is in the patients best interests?
1. What are the patient's **past/present** wishes or feelings relating to the decision?
2. What are the patient's values and beliefs relating to the decision?
3. What are the risks/benefits of each option?
4. Consider other factors e.g. future implications and safety concerns.
Should be **verified with consultee ie family member or friend**
116
Outline the two stages needed to gauge mental capacity
1 - is there impairment of or disturbance of function in a person's brain or mind?
2 is the impairment sufficient to constitute a loss of capacity? 4 components
117
What are the four components around capacity to make a decision that are required in order to have capacity?
Can teh patient understand teh info required to make an decision - **RECIEVE**
Can they retain the info long enough to make a decision - **RETAIN**
Can they weigh up the info? **RATIONALISE**
Can they communicate the decision back **RELATE BACK**
4 Rs
118
What are the 5 principles of the Mental Capacity Act?
**Assume capacity** – person assumed to have capacity until proven otherwise
**Maximise decision-making capacity** – all practical support to help a person make a decision should be given
**Freedom to make seemingly unwise decisions** – an apparently unwise decision in itself does not prove incapacity
**Best interests** – all decisions taken on behalf of the person must be in their best interests
**Least restrictive option** – when deciding on another person’s behalf, chose the decision that interferes the least with the person’s rights and freedom of action while still achieving goal
119
What are some antibiotics you wnat to avoid in pregnancy
Antibiotics Contraindicated in Pregnancy:
Tetracyclines (e.g., Doxycycline): Tooth discolouration, bone development issues
Fluoroquinolones (e.g., Ciprofloxacin): Joint malformations, cartilage development interference
Trimethoprim (alone): Neural tube defects (folate metabolism disruption)
Aminoglycosides (e.g., Gentamicin): Ototoxicity, nephrotoxicity
Chloramphenicol: Bone marrow suppression, aplastic anemia
Metronidazole (1st trimester): Potential teratogenicity
120
What common causes of faltering growth do you need to rule out in GP
Coeliac disease
Undiagnosed UTIs - get a urine sample
121
Causes of faltering growth: give examples of inadequate calorie intake.
1. Impaired suck/swallow. - eg Cleft palate, cerebral palsy
2. Inadequate availability of food.
3. Psychosocial deprivation.
4. Exclusion diets e.g. veganism
Infant difficult to feed – resists feeding or disinterested
* Conflict over feeding, intolerance of normal feeding behaviour, e.g.
messiness, throwing food around, leading to an early cessation of meals
122
Causes of faltering growth: give examples of malabsorption.
1. Coeliac disease.
2. Pancreatic disease e.g. CF.
3. Liver disease.
4. Enteropathy e.g. infective causes - giardia.
5. Cows milk protein intolerance.
123
Causes of faltering growth: give an example of inadequate retention.
Vomiting e.g. severe GORD, pyloric stenosis.
124
Causes of faltering growth: give example increased calorie requirements.
1. Chronic illness e.g. CHD, CKD, CF.
2. Thyrotoxicosis.
3. Malignancy.
125
What is the management for cows milk protien allergy?
Breast feeding mothers should avoid dairy products
Replace formula with special hydrolysed formulas designed for cow’s milk allergy
– If severe symptoms –> use amino-acid based formula (AAF) milk (elemental formulas) - Pepti Junior
*Hydrolysed formulas contain cow’s milk, however the proteins have been broken down so that they no longer trigger an immune response* -
126
tests for faltery growth
Anthropometry – Height, weight, head circumference (growth chart)
Dietary & Feeding History – Caloric intake, feeding difficulties
Blood Tests:
FBC – Anemia, infection
Electrolytes & renal function – Dehydration, kidney issues
Thyroid function – Hypothyroidism
Coeliac screen (anti-tTG) – Malabsorption
Liver function tests – Liver disease
Iron studies – Iron deficiency anemia
Urinalysis – Infection, dehydration, metabolic issues
Stool Tests – Infection (culture, ova & parasites), malabsorption (fecal calprotectin)
Genetic Testing – If syndromic features present
Chest X-ray – Lung disease, structural abnormalities
Cardiac Evaluation – ECG/Echo for congenital heart disease
Growth Hormone Tests – IGF-1, GH stimulation (if GH deficiency suspected)
127
: What are the key red flag symptoms of throat cancer?
🚨 Red Flag Symptoms (NICE Guidelines)
✅ Persistent unexplained hoarseness for ≥3 weeks
✅ Unexplained neck lump
✅ Dysphagia (difficulty swallowing)
✅ Unexplained persistent sore throat or throat pain
✅ Stridor (noisy breathing due to airway obstruction)
✅ Unexplained persistent cough (especially with haemoptysis)
✅ Unintentional weight loss + other symptoms
🚨 High-Risk Patient Factors
Smoker (especially heavy smokers)
Excess alcohol intake
HPV infection (linked to oropharyngeal cancer)
History of head & neck cancer
Persistent gastro-oesophageal reflux (GORD)
If any of the above are present, an urgent ENT referral is needed for laryngoscopy and further assessment.
128
What are the main risk factors for throat cancer?
Smoking, alcohol, HPV, GORD, occupational exposure, family history.
129
What are the most common benign causes of hoarseness in primary care?
Laryngitis, vocal strain, GORD, postnasal drip, smoking.
130
What is keratosis pilaris
A common, benign skin condition causing rough, small bumps due to keratin buildup in hair follicles.
131
What are the key features of keratosis pilaris?
: What areas of the body are most commonly affected?
Small, rough, flesh-colored or red bumps that feel like sandpaper and are usually asymptomatic or mildly itchy.
Upper arms, thighs, cheeks, and buttocks.
132
What are the treatment options for keratosis pilaris?
Moisturizers, gentle exfoliation, urea or lactic acid creams, and avoiding harsh soaps
Often improves with age but can persist into adulthood.
133
Causes of peripheral neuropathy (numbness/tingling in hands and feet)
Diabetes mellitus
Vitamin deficiencies
B12 (esp. pernicious anaemia)
B1 (thiamine) and B6
Alcohol excess
Drugs/toxins
Chemotherapy (e.g. vincristine, cisplatin), Isoniazid, nitrofurantoin, amiodarone, Heavy metals (lead, arsenic)
Chronic kidney disease (uraemia)
Hypothyroidism
Autoimmune diseases
SLE, RA, Sjögren’s Guillain-Barré syndrome
134
Shoulder pain causes - give cause, presentation and signs of Rotator cuff tendinopathy
🧬 Cause: Overuse, repetitive overhead activity, age-related wear (esp. supraspinatus)
📋 Presentation: Dull lateral shoulder ache, worse with overhead movement, painful arc
✅ Tests:
Painful arc (60–120° abduction)
Empty Can test (supraspinatus)
135
Shoulder pain causes - give cause, presentation and signs of subacromial impingement
🧬 Cause: Compression of rotator cuff tendons beneath the acromion
📋 Presentation: Sharp pain on overhead movement, difficulty sleeping on affected side
Painful Arc
Pain between 60° and 120° of arm abduction, Weakness in shoulder external rotation
136
Shoulder pain causes - give cause, presentation and signs of rotator cuff tea
. Rotator Cuff Tear
🧬 Cause: Trauma (fall/lifting) or chronic degeneration, especially in older adults
📋 Presentation: Weakness lifting arm, night pain, difficulty initiating abduction
✅ Tests that are postive
Empty Can
External rotation against resistance
137
Shoulder pain causes - give cause, presentation and signs of frozen shoulder
🧬 Cause: Idiopathic, post-injury, diabetes-related
📋 Presentation: Gradual onset of global stiffness and pain, esp. in external rotation
✅ Tests:
Global restriction of both active & passive ROM
Especially limited external rotation
138
What are the symptoms of GCA?
Main symptom is **headache that us unilateral and around forehead and temple.**
Irreversible painless complete sight loss
Jaw claudication
Scalp tenderness may be noticed when brushing hair
139
What are the primary investigations of GCA?
1st line:
**INCREASED ESR** - ELEVATED IN 83% OF CASES- should be more than 100
increase CRP and platelets
ANCA Negative
Temporal Artery biopsy - diagnostic
ultrasound scan
Fundoscopy
palpate temporal artery - tender, may be absent pulse
Picture - diagnostic criteria
140
What is the management for giant cell arthritis?
What may happen if a patient with GCA was to stop taking these medication immediately?
1st Line:
Corticosteroids - Oral Prednisolone - eitehr 40 or 60
urgnet US referral
vision - ophthalmology input
refer , having given steroids
If you stop steroid doses abruptly, could cause an **Adrenal crisis**
141
things to think about w long term steroids in GCA/PMR
get around 5mg pred
diabetes risk
osteoporosis risk
long term steroid use - adrenal crisis
142
Name some risk factors, and potential triggers of a migraine
- **Family history**
- **Female gender**: migraines are three times more common in women
- **Obesity**
- **Triggers**: CHOCOLATE
- **Ch**ocolate
- **O**ral **C**ontraceptive
- Alcoh**ol**
- **A**nxiety
- **T**umult - Loud noise
- **E**xercise
- **Other important triggers** include tiredness, lack of food, dehydration, menstruation, red wine and bright lights, under of over sleeping
143
How are migraines diagnosed?
Clinical Dx unless pathology is suspected where you do tests to exclude DDx, investigating red flags:
**CT/MRI red flags** ie. Indications
- Worst/severe headache ie. Thunderclap
- Change in pattern of migraine
- Abnormal neurological exam
- Onset >50yrs
- Epilepsy
- Posteriorly located headache
**Lumbar puncture** indications
- Thunderclap headache
- Severe, rapid onset headache/ progressive headache/ unresponsive
headache
144
What are the treatments for Migraines?
Conservative - Avoid Triggers
**ACUTE MANAGEMENT**
Mild - Paracetamol/NSAIDs - ibuprofen (take at aura stage) -
Severe - Triptans - **sumatriptan** (only take when having headache)
Anti-emetics - metoclopramide - prokinetic, due to gastric stasis or proclopremazine
ARB - Candesartan
Avoid use of Opiates
cant give triptans to people on SSRIs, and heart disease (is a vasoconstrictor)
145
What are some preventative measures you can give to help stop migraines occurring?
Required if >2 attacks per month OR require acute meds >2x per week
Beta blockers eg. **propranolol** (lowers max HR, cold peripheries)
**TCAs eg**. **amitriptyline**
Anti-convulsant eg. **Topiramate**
*Propranolol is preferable to topiramate in women of childbearing age for migraine prophylaxis*
Candesartan
Botox injections = **generally used for the treatment of chronic migraines (15 or more days per month),**
- CAS patient!
146
What are some triggers of tension headaches?
**STRESS** - MAIN RISK FACTOR/TRIGGER
Sleep deprivation
Bad posture
Hunger
Eyestrain
Anxiety
Conflict
Overexertion
Depression
Clenched jaw
Noise
147
What is the some of the features of the typical diagnostic criteria seen in tension headaches?
Bilateral, mild to moderate intensity pain
Not aggravated by exercise
No nausea or vomiting (anorexia may occur)
No more than one of photophobia and phonophobia
148
What a medication overuse headache, how it may present, and the management of it
Medication Overuse Headache (MOH): Headache caused by excessive use of acute headache medications (e.g., painkillers).
Presentation: Chronic, daily or near-daily headache in individuals frequently using analgesics or triptans.
Management: Gradual withdrawal of overused medication, supportive care, and preventive headache treatment.
Medication overuse is typically defined as:
Simple analgesics (e.g., paracetamol, NSAIDs): >15 days/month.
Combination analgesics, triptans, ergotamines, or opioids: >10 days/month.
149
what are some headache red flags
Red Flag Headache Symptoms ("SNOOP"):
S: Systemic symptoms (fever, weight loss, cancer, HIV)
N: Neurologic signs (focal deficits, seizures, AMS)
O: Sudden onset (thunderclap, peak in <1 min)
O: Onset after age 50
P: Pattern change (first/worst headache, different character)
Bonus Red Flags:
Papilledema
Positional or Valsalva-triggered
Trauma
Pregnancy/postpartum
Temporal artery tenderness
150
When would you do a 2 week wait referral for headache?
2-Week Wait Referral (Urgent Cancer Pathway):
Refer if:
New headache with:
New-onset neurological deficit
Change in personality or cognitive function
Headache + history of cancer (esp. lung, breast, melanoma)
Progressive focal neurological signs
Headache + papilledema
Seizure or persistent vomiting
Suspected brain tumour or space-occupying lesion
151
when would you refer to a neurologist for headaches, and what are some investigations you could use
Investigations may include:
CT head (non-contrast): for acute onset or trauma
MRI brain: for subacute/chronic or focal neurological signs
Lumbar puncture: if SAH suspected but CT is negative, or for suspected meningitis
ESR/CRP: if temporal arteritis suspected
Visual field testing: if concern about pituitary tumor or raised ICP
When to Refer for Specialist Management (CS09)
Neurology referral:
New daily persistent headache
Cluster headaches
Medication overuse headache
Trigeminal neuralgia not responding to first-line treatment
Chronic migraine not responding to prophylaxis
152
What is the management for tension headaches
Acute:
Paracetamol or NSAIDs (e.g. ibuprofen)
Avoid opioids & combo analgesics
Preventive (chronic/frequent):
Amitriptyline (10–30mg nocturnal)
Consider nortriptyline, venlafaxine
Non-Pharm:
Stress management (CBT, relaxation)
Physio, posture correction
Sleep hygiene
Regular exercise
Headache diary
153
What is TMJ disorder and what are the key types?
TMJ disorder is dysfunction or pain in the temporomandibular joint and/or muscles of mastication.
Key types:
- Myofascial pain (muscle-based)
- Internal derangement (e.g. disc displacement)
- Degenerative joint disease (e.g. osteoarthritis)
154
What are the classic symptoms of TMJ disorder?
Symptoms:
- Jaw pain or tenderness
- Clicking/popping sounds
- Limited jaw opening or locking
- Ear symptoms (fullness, tinnitus, referred pain)
- Headache (especially temporal)
On examination:
- Tenderness over TMJ and masseter/temporalis
- Deviation on opening
- Joint crepitus or clicking
- Reduced interincisal opening (<40mm = limited)
155
What are common causes or risk factors for TMJ disorder?
Causes/Risk factors:
- Bruxism (teeth grinding/clenching)
- Stress (muscle tension)
- Poor posture
- Jaw trauma
- Joint hypermobility
- Malocclusion (controversial role)
156
How is TMJ disorder managed conservatively?
Management:
- NSAIDs
- Moist heat or cold packs
- Soft diet, jaw rest
- Stress reduction
- Jaw exercises, posture correction
- Occlusal splints (night guards)
On follow-up: Look for improved range, reduced tenderness, fewer joint noises.
157
What red flags or advanced treatments should be considered in TMJ disorder?
Red flags:
- Persistent jaw locking
- Facial asymmetry or bite changes
- Neuropathic-type pain
Advanced treatments:
- Botox for muscle overactivity
- Arthrocentesis or surgery (last resort)
- Cognitive behavioral therapy
- Referral to orofacial pain or maxillofacial specialist
158
TIred all the time bloods to do in GP
Basic Fatigue Screen:
Full Blood Count (FBC) – to assess for anemia, infection, or hematological abnormalities.
Urea & Electrolytes (U&Es) – to evaluate kidney function and electrolyte balance.
Liver Function Tests (LFTs) – for hepatic causes of fatigue.
Thyroid Function Tests (TFTs) – to rule out hypothyroidism.
C-Reactive Protein (CRP) or ESR – for underlying inflammation or infection.
HbA1c – to screen for diabetes or pre-diabetes.
Ferritin – iron stores, especially in menstruating women or if FBC shows low MCV.
Vitamin B12 and Folate – for deficiency-related anemia or neurological fatigue.
Vitamin D – commonly deficient and contributes to fatigue.
**Coeliac Screen** - Bimodal presentation (can present at 50), atypical prezsnetiation
Monospot or EBV serology in younger patients or with recent viral symptoms.
HIV and Hepatitis screen if risk factors present.
159
160
What is the management of radiculopathy?
Medications, like nonsteroidal anti-inflammatory drugs, opioid medicines or muscle relaxants, to manage the symptoms
Weight loss strategies to reduce pressure on the problem area
Physical therapy to strengthen the muscles and prevent further damage
Steroid injections to reduce inflammation and relieve pain
Srugery to reduce pressure on nerve root
161
What are the most common nerve roots affected in a radiculopathy, in the lower limb?
Therefore, what will be affected?
L5 Dorsum or top of foot/big toe Dorsiflexion (stand on
heels)
S1 - all the S's - Side of foot sole of foot, Small (little) toe area
Plantar flexion (stand on toes)
Ankle jerk
162
What are common causes of sciatica?
Herniated lumbar disc, spinal stenosis, piriformis syndrome, spondylolisthesis, trauma, or tumors compressing the sciatic nerve.
163
What tests are used to diagnose sciatica?
Physical exam (e.g., straight leg raise test), MRI, CT scan, and electromyography (EMG) to assess nerve function and compression.
164
What are typical symptoms of sciatica?
Radiating pain from lower back through buttock and down leg, numbness, tingling, muscle weakness, and worsened pain with sitting or movement.
165
What are treatment options for sciatica?
1. Conservative (First-line):
NSAIDs (e.g., ibuprofen, naproxen)
Activity modification (avoid prolonged sitting, heavy lifting)
Physical therapy (core strengthening, stretching, McKenzie exercises)
Heat/Ice therapy
2. Adjunctive Treatments:
Oral corticosteroids (short course)
Muscle relaxants (e.g., cyclobenzaprine)
Neuropathic pain agents (e.g., gabapentin, pregabalin, amitriptyline)
3. Interventional:
Epidural corticosteroid injections (for persistent pain >6 weeks)
4. Surgical (if red flags or no improvement after 6–12 weeks):
Microdiscectomy (for herniated disc)
Laminectomy (for spinal stenosis)
166
What are the key differential diagnoses for numbness and tingling in the hands?
Carpal tunnel syndrome, ulnar nerve entrapment, cervical radiculopathy, diabetic neuropathy, B12 deficiency, hypothyroidism, multiple sclerosis, thoracic outlet syndrome, anxiety-related paresthesia.
167
Causes of Polyneuropathy
(what drug used for diabetes induced polyneuropathy)?
Common Causes of Polyneuropathy
Metabolic:
Diabetes mellitus (most common cause)
**Chronic kidney disease** (uremic neuropathy)
Hypothyroidism
Nutritional Deficiencies:
Vitamin B12 deficiency
**Thiamine (B1) deficiency** – often due to alcoholism
Vitamin E deficiency
Toxic:
Alcohol
Chemotherapy agents (e.g., vincristine, cisplatin)
Heavy metals (lead, arsenic, mercury)
**Isoniazid or metronidazole (drug-induced)**
Infectious:
HIV
Hepatitis B or C
Lyme disease
Autoimmune/Inflammatory:
Guillain-Barré syndrome (acute demyelinating polyneuropathy)
Vasculitic neuropathy (e.g., PAN, SLE)
Hereditary:
Charcot-Marie-Tooth disease
***Duloxetine treats diabetic neuropathy by increasing serotonin and norepinephrine in central pain pathways, enhancing inhibition of peripheral pain signals. It reduces neuropathic pain independent of its antidepressant effects.***
168
Common causes of mononeuropathy
Compression/Entrapment Neuropathies (Most Common):
Carpal tunnel syndrome – median nerve at wrist
Ulnar nerve entrapment – at elbow or wrist
Radial nerve palsy – "Saturday night palsy"
Peroneal nerve palsy – at fibular head, foot drop
Bells Palsy
Trauma:
Nerve injury due to fractures, dislocations, or lacerations
Iatrogenic injury during surgery or injection
Ischemia:
Mononeuritis multiplex (vasculitis affecting individual nerves asymmetrically)
Diabetes-related ischemic mononeuropathy
Infectious:
Herpes zoster (shingles) affecting peripheral nerves
HIV-associated mononeuropathy
Tumors/Masses:
Nerve compression by lipomas, ganglion cysts, or malignancies
169
causes for nausea in cancer patients
3 Bs
Bowel (GI infection, obstruction,
Brains (brain mets, inner ear, vertigo
Bloods/Biochemistry and treatments, (high calcium, low sodium, high
Concise Causes of Nausea in a Breast Cancer Patient:
Chemotherapy – Direct gastric mucosal irritation or central (CNS) stimulation.
Radiation therapy – Especially if near upper abdomen or CNS.
Opioids – Common side effect due to CNS and GI receptor activation.
Cancer-related metabolic disturbances – e.g., hypercalcemia, liver metastases.
Gastrointestinal involvement – Tumor infiltration or obstruction.
Brain metastases – Increased intracranial pressure or direct emesis center involvement.
Psychological factors – Anxiety or anticipatory nausea.
Infections – Opportunistic or treatment-related (e.g., candidiasis, gastritis).
Medications – e.g., antibiotics, antidepressants, hormonal therapies (e.g., tamoxifen).
Gastroparesis – Possibly due to autonomic neuropathy or medication effects
170
Side effects, MOA and best use for Metoclopramide
MOA: D2 antagonist; weak 5-HT3 antagonist; prokinetic (↑ gastric emptying).
Best for: Gastroparesis, chemotherapy-induced nausea, postoperative nausea, migraine-related nausea.
CIs: Parkinson’s disease, bowel obstruction, epilepsy.
Side Effects: Extrapyramidal symptoms (EPS), tardive dyskinesia, sedation, diarrhea.
171
Side effects, MOA and best use for Cyclizine
MOA: H1 antihistamine with anticholinergic properties.
Best for: Motion sickness, vestibular nausea, raised ICP-related nausea, opioid-induced nausea.
CIs: Glaucoma, urinary retention, severe heart failure.
Side Effects: Dry mouth, drowsiness, dizziness, anticholinergic effects (confusion, constipation).
172
Side effects, MOA and best use for ondanestron
MOA: 5-HT3 receptor antagonist (central and peripheral).
Best for: Chemotherapy or radiation-induced nausea, postoperative nausea.
CIs: Congenital long QT syndrome.
Side Effects: QT prolongation, headache, constipation, serotonin syndrome (rare).
173
Side effects, MOA and best use for Haloperidol
MOA: Potent D2 receptor antagonist (central).
Best for: Refractory nausea (especially in palliative care), opioid/metabolic causes.
CIs: Parkinson’s disease, QT prolongation, severe CNS depression.
Side Effects: EPS, QT prolongation, sedation, agitation.
174
Outline different types of distribution for skin lesion
Note the distribution of the lesion(s):
Acral distribution: distal areas including the hands and feet (e.g. hand, foot and mouth disease)
Central distribution: over chest and back (photo-protected)
Peripheral distribution: over arms and legs (more sun-exposed)
Sun-exposed (photo) distribution: areas of high sun exposure will have a higher incidence of lesions caused by chronic sun damage (face, ears, nose, arms, lower legs). These areas are more likely to present with worrying pigmented lesions later in life. Young people are more likely to have new, worrying pigmented lesions in minimally photo-damaged areas.
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Outline ABCDE approach for skin lesions
Asymmetry
Asymmetry of a lesion typically refers to networks, patterns, markings, colours or features that are not regularly distributed through the entire lesion.
Border
Benign lesions typically have a smooth and regular border.
Colour
Benign lesions typically demonstrate uniform colour throughout.
describe the colours as you see them and keep it simple (e.g. light brown, mid-brown, dark brown).
Diameter
Evolution
A history of abnormal evolution of the lesion is one of the most concerning risk factors for potential malignancy.
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What ABCDE features in skin lesion assessment are concerning for malignancy?
If an irregular border is present (e.g. streaks, wavy edge) this increases the likelihood of malignancy.
The presence of more than 2 colours increases the likelihood of malignancy.
Colours within pigmented lesions such as pinks, blues, greys, whites or deep blacks increase the likelihood of malignancy.
A lesion with a diameter of 6mm or more increases the likelihood of malignancy.
Lesions that are growing quickly and/or changing in appearance over a short time period are highly concerning for malignancy.
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Give some features of lesions that are benign and should not be confused with a melanoma for example seborrhoeic keratoses
described as a stuck-on papule, nodule, or plaque.
Cerebriform pattern: cerebriform, or brain-like, describes the gyri and sulci of the stuck-on plaque or nodule
Keratin pearls: these go hand in hand with pseudo-comedones and are small, pale, round structures that dot a keratosis.
Shiny or wart-like: seborrhoeic means “greasy”. This refers to the smoother, more shiny keratoses.
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Features of Basal cell carcinoma
Basal Cell Carcinoma (BCC)
Growth: Slow-growing, locally invasive, rarely metastasizes.
Appearance:
Pearly or translucent nodule
Rolled edges with central ulceration ("rodent ulcer")
Telangiectasia
May be pigmented (especially in darker skin)
Common sites: Sun-exposed areas — head, neck, upper trunk
Symptoms: Usually painless; may bleed or crust
Subtypes: Nodular (most common), superficial, morphoeic (infiltrative)
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What are the signs and symptoms of a squamous cell carcinoma?
SCC of the skin begins as a small nodule and as it enlarges the center becomes necrotic and sloughs and the nodule turns into an ulcer
Growth: Faster growing; potential to metastasize, especially on high-risk sites.
Appearance:
Firm, scaly or keratotic papule/nodule
May ulcerate with indurated edges
Crusting or bleeding common
Common sites: Sun-exposed areas — face, ears, scalp, hands; also chronic wounds or scars
Symptoms: Often tender or painful
Risk factors: Immunosuppression, chronic UV exposure, HPV, chronic inflammation
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Squamous Cell carcinoma - what is bowens Disease?
Bowen's disease is essentially equivalent to and used interchangeably with cSCC in situ, when not having invaded through the basement membrane
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How do you diagnose and manage cutaneous squamous cell carcinomas?
Diagnose with Biopsy
removed with surgery. A few selected cases are treated with topical medication. Surgical excision with a free margin of healthy tissue is a frequent treatment modality. Radiotherapy, given as external beam radiotherapy or as brachytherapy (internal radiotherapy), can also be used to treat cSCC.
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What is a basal cell carcinoma, and what are the features of it
Originates from basal keratinocytes in the lower epidermis. Basal cell carcinomas are slow-growing and rarely metastasize,
Appearance:
**Pearly or translucent nodule**
Rolled edges with central ulceration ("rodent ulcer")
**Telangiectasia**
May be pigmented (especially in darker skin)
Common sites: Sun-exposed areas — head, neck, upper trunk
Symptoms: Usually painless; may bleed or crust
Subtypes: Nodular (most common), superficial, morphoeic (infiltrative)
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What is Acitinic keratosis ? what is its link wiht bowens and SCC
solar keratosis, is a pre-malignant lesion of epidermal keratinocytes caused by chronic sun exposure.
AKs are considered early in situ squamous cell carcinomas (SCCs) and can progress to invasive SCC if left untreated. Approximately 82% of cutaneous SCCs arise from AKs. Bowen's disease, also known as SCC in situ, represents a more advanced stage of keratinocyte dysplasia compared to AK but is still confined to the epidermis.
~15–25% in middle-aged adults in the UK
Up to 60% in elderly Caucasian men
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What are some features of Acinitic keratosis? What is the mangaement of it?
Clinical Features
Rough, scaly patches on sun-exposed skin (e.g., face, scalp, forearms, dorsum of hands)
Flesh-coloured, pink, or red, often with a dry, sandpaper-like texture
May be asymptomatic or mildly itchy/tender
Lesions can be single or multiple
Assess: sun exposure history, immunosuppression, lesion characteristics
Treatment options:
Cryotherapy (liquid nitrogen) – first-line for isolated lesions
Topical 5-**fluorouracil**, **(Efudix Cream)** imiquimod, diclofenac gel – for field treatment
Photodynamic therapy – for extensive or recurrent lesions
*can cause lesion become very red and angry as put cream on, need to educate patient about this*
Referral: Dermatology if:
Diagnostic uncertainty
Suspicion of progression to Bowen’s or SCC
Extensive field cancerisation
